Stachyose modulates gut microbiota and alleviates dextran sulfate sodium-induced acute colitis in mice

水苏糖调节小鼠肠道菌群并缓解葡聚糖硫酸钠诱发的急性结肠炎

阅读:6
作者:Liwen He, Feiran Zhang, Zhengyang Jian, Jiachen Sun, Jiamin Chen, Vuekhang Liapao, Qing He

Aim

Ulcerative colitis (UC) has been implicated to imbalanced enteric flora and reduced microbial diversity. Stachyose is a kind of natural prebiotic which favorably modulate the composition of the gut microbiota. The present study aims to investigate the effects of stachyose on inflammatory levels and gut microbiota of acute colitis mice. Materials and

Conclusions

Our results suggested that stachyose increased beneficial microbiota and bacterial diversity to alleviate acute colitis in mice, which might be a new promising option to UC patients.

Methods

In this study, the mice were randomly divided into four groups: (1) control group; (2) stachyose group; (3) dextran sulfate sodium (DSS) group; (4) stachyose + DSS group. Hemotoxylin and Eosin (H and E) staining was performed for the distal colon to examine the inflammation and tissue damage. The inflammatory cytokines including IL-6, IL-10, IL-17a, and TNF-α in serum were determined by ELISA assay. The differences in the gut microbiota were analyzed by 16S rDNA gene sequencing.

Results

Histological assay showed that the stachyose treatment significantly reduced the lesions of the colon in DSS-induced colitis. And the upregulated inflammatory cytokines induced by DSS were significantly inhibited by stachyose treatment. Additionally, the sequencing analysis showed that the stachyose changed the gut microbiota composition with a higher level of Akkermansia, as well as selectively increasing some probiotics, including Lactobacillus. Conclusions: Our results suggested that stachyose increased beneficial microbiota and bacterial diversity to alleviate acute colitis in mice, which might be a new promising option to UC patients.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。